Persistence of Highly Pathogenic Avian Influenza Viruses in Natural Ecosystems

Understanding of ecologic factors favoring emergence and maintenance of highly pathogenic avian infl uenza (HPAI) viruses is limited.Although low pathogenic avian infl uenza viruses persist and evolve in wild populations, HPAI viruses evolve in domestic birds and cause economically serious epizootics that only occasionally infect wild populations.We propose that evolutionary ecology considerations can explain this apparent paradox.Host structure and transmission possibilities differ considerably between wild and domestic birds and are likely to be major determinants of virulence.Because viral fi tness is highly dependent on host survival and dispersal in nature, virulent forms are unlikely to persist in wild populations if they kill hosts quickly or affect predation risk or migratory performance.Interhost transmission in water has evolved in low pathogenic infl uenza viruses in wild waterfowl populations.However, oropharyngeal shedding and transmission by aerosols appear more effi cient for HPAI viruses among domestic birds. W ild birds, especially waterbirds of the orders An-seriformes (ducks, geese, and swans) and Charadriiformes (gulls, terns, and waders), are natural hosts for infl uenza A (avian infl uenza) viruses.Avian infl uenza viruses are classifi ed on the basis of genetic, antigenic, and structural characteristics of hemagglutinin and neuraminidase proteins.These proteins are involved in binding of virus to host cells and release of new virions from these cells, respectively.Sixteen hemagglutinins (H1-H16) and 9 neuraminidases (N1-N9) have been described.For avian infl uenza viruses of subtypes H5 and H7, there are 2 types of virulence: low pathogenic avian infl uenza (LPAI) virus generally produces benign intestinal tract or respiratory infections; highly pathogenic avian infl uenza (HPAI) virus generally produces multiorgan systemic infections.LPAI viruses naturally infect wild waterbirds according to host species, age, immune status, feeding behavior, premigration aggregation, and aquatic survival of the virus.Long-term studies in Europe and North America also identifi ed seasonal variation in prevalences of infection of LPAI virus and circulating subtypes.HPAI viruses primarily infect poultry in which viruses of subtypes H5 and H7, presumably from wild birds or contact with their derivatives, sporadically switch to highly virulent strains.At the end of the 19th century, a disease that caused high mortality rates and spread rapidly was described in domestic birds in Italy.This fowl plague spread through Europe in the early 20th century, most likely through trading of domestic birds.In 1955, the pathogen responsible for the disease was classifi ed as an infl uenza A virus, and its relationship to human infl uenza viruses was recognized.Domestic birds have been affected by recurrent outbreaks of HPAI viruses, generally limited to localized geographic areas but responsible for high mortality rates and substantial economic losses.In contrast, wild birds have rarely been involved in HPAI virus infections.Before 1996, only 1 HPAI virus outbreak was documented in the wild, resulting in the death of ≈1,300 common terns (Sterna hirundo) in South Africa (1).Since then, emergence and spread of the HPAI virus lineage from Asia (H5N1), fi rst discovered in domestic geese in southern People's Republic of China in 1996, has been responsible Persistence of Highly Pathogenic Avian Infl uenza Viruses in Natural Ecosystems

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